摘要
目的应用Aβ25-35诱导并建立痴呆大鼠模型,观察人参皂苷Rb1对海马神经元凋亡的保护作用。方法选取Sprague Dawley大鼠42只,采用随机数字表法分为模型组、治疗组及正常组,每组14只。模型组和治疗组建立Aβ25-35诱导痴呆大鼠模型,治疗组大鼠实验前、造模后7 d给予20 mg/(kg·d)人参皂苷Rb1,模型组和正常组给予等体积的生理盐水灌胃。建立模型喂养7 d后,Morris水迷宫实验检测大鼠学习记忆力进行后处死大鼠,末端标记法(TUNEL)检测大鼠海马神经元的凋亡,免疫组织化学法检测大鼠海马神经元细胞周期蛋白D1、Fas、Fas L水平及凋亡相关基因Survivin、Bcl-2、Bax及p53蛋白表达水平。结果模型组大鼠学习记忆力较正常组大鼠明显降低,而Rb1治疗组大鼠的学习记忆力较模型组明显改善(P<0.05);治疗组大鼠细胞周期蛋白D1阳性率为(38.60±5.02)%,高于模型组[(19.81±5.74)%]均低于正常组,差异有统计学意义(P<0.05);治疗组大鼠凋亡细胞阳性率为(47.33±7.92)%,低于模型组[(72.68±9.80)%],均高于正常组,差异有统计学意义(P<0.05);治疗组Fas、Fas L和Bax蛋白阳性率分别为(56.42±8.17)%、(44.27±6.35)%和(52.09±7.10)%,低于模型组,均高于正常组,差异有统计学意义(P<0.05);治疗组Bcl-2、Survivin和p53蛋白阳性率分别为(61.53±5.92)%、(53.19±8.24)%和(59.16±8.79)%,高于模型组,均低于正常组,差异有统计学意义(P<0.05)。结论人参皂苷Rb1对Aβ25-35诱导的痴呆大鼠记忆力及认知功能具有保护作用,降低海马神经元的损伤和凋亡,并通过下调Fas、Fas L和Bax蛋白的表达水平,增加Bcl-2、Survivin和p53蛋白的阳性表达而发挥作用。
[Objective] To induce and establish the dementia rat model by Aβ25-35, and to observe the protective effect of ginsenoside Rbl on the apoptosis of hippocampal neurons. [Methods] Forty-two SD rats were randomly divided into three groups by the random number table method, with 14 rats in each group. The rats in the model and Rbl treatment groups were treated with Aβ25-35 for induction of dementia model. The rats in the Rbl treatment group were given Rbl 20 mg/（kg·d） before and one week after model establishment and those in the normal and model groups were given equal volume of normal saline by gavage. They were raised for 7 days. Morris water maze was used to detect learning and memory ability of the rats. Then the rats were sacrificed. TUNEL method was used to detect hippoeampal neuron apoptosis. Immunohis- tochemistry was used to detect the eyclin D1, Fas and FasL levels, and apoptosis-related survivin, Bel-2, Bax and p53 protein expression levels of hippoeampal neurons. [Results] Learning and memory ability of the rats in the model group decreased compared with that in the normal group. Learning and memory ability of the Rbl treatment group was significantly improved compared that of the model group （P〈0.05）. Cyelin D1 posi- tive rate of the Rbl treatment group was （38.60 ± 5.02）%, which was significantly higher than that of the model group [（19.81 ± 5.74）%]; and eyelin D1 positive rate of both groups was significantly lower than that of the normal group （P 〈 0.05）. TUNEL positive rate of the Rbl treatment group was （47.33 ± 7.92）%, which was significantly lower than that of the model group [（72.68 ± 9.80）%]; both were significantly higher than that of the normal group （P〈0.05）. Fas, FasL and Bax protein positive rates of the Rbl treatment group were （56.42 ± 8.17）%, （44.27 ±6.35）% and （52.09 ± 7.10）% respectively, which were significantly lower than those of the model group, but significantly higher than those of the normal group （P〈 0.05）. Bcl-
出处
《中国现代医学杂志》
CAS
北大核心
2015年第35期33-36,共4页
China Journal of Modern Medicine
